Comparison of Domain Nucleation Mechanisms in a Minimal Model of Shoot Apical Meristem

TL;DR

This paper compares two mechanisms for stem cell domain formation in the shoot apical meristem, showing that a bistable-switch model is more biologically plausible than the traditional Turing mechanism.

Contribution

It introduces and analyzes a bistable-switch model for SAM nucleation, challenging the assumptions of differential diffusivity in Turing models.

Findings

Bistable-switch mechanism can explain SAM domain formation without differential diffusivity.

The bistable model acts as localized switches driven by peptide hormones.

Compared models show the bistable mechanism aligns better with biological evidence.

Abstract

Existing mathematical models of the shoot apical meristem (SAM) explain nucleation and confinement of a stem cell domain by Turing's mechanism, assuming that the diffusion coefficients of the activator (WUSCHEL) and inhibitor (CLAVATA) are significantly different. As there is no evidence for this assumption of differential diffusivity, we recently proposed a new mechanism based on a bistable switch model of the SAM. Here we study the bistable-switch mechanism in detail, demonstrating that it can be understood as localized switches of WUSHEL activity in individual cells driven by a non-uniform field of a peptide hormone. By comparing domain formation by Turing and bistable-switch mechanisms on a cell network, we show that the latter does not require the assumptions needed by the former, which are not supported by biological evidences.